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J. Biol. Chem., Vol. 275, Issue 47, 37137-37149, November 24, 2000
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From the We used whole cell recording to evaluate
functional expression of the intermediate conductance
Ca2+-activated K+ channel,
IKCa1, in response to various mitogenic stimuli. One to two
days following engagement of T-cell receptors to trigger both PKC- and
Ca2+-dependent events, IKCa1
expression increased from an average of 8 to 300-800 channels/cell.
Selective stimulation of the PKC pathway resulted in equivalent
up-regulation, whereas a calcium ionophore was relatively ineffective.
Enhancement in IKCa1 mRNA levels paralleled the
increased channel number. The genomic organization of
IKCa1, SKCa2, and SKCa3 were
defined, and IKCa and SKCa genes were found to
have a remarkably similar intron-exon structure. Mitogens enhanced
IKCa1 promoter activity proportional to the increase in
IKCa1 mRNA, suggesting that transcriptional mechanisms underlie channel up-regulation. Mutation of motifs for AP1 and Ikaros-2
in the promoter abolished this induction. Selective Kv1.3 inhibitors ShK-Dap22, margatoxin, and correolide suppressed
mitogenesis of resting T-cells but not preactivated T-cells with
up-regulated IKCa1 channel expression. Selectively blocking
IKCa1 channels with clotrimazole or TRAM-34 suppressed
mitogenesis of preactivated lymphocytes, whereas resting T-cells were
less sensitive. Thus, Kv1.3 channels are essential for
activation of quiescent cells, but signaling through the PKC pathway
enhances expression of IKCa1 channels that are required for
continued proliferation.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF305731-AF305735 and AH009923.
Up-regulation of the IKCa1 Potassium Channel
during T-cell Activation
MOLECULAR MECHANISM AND FUNCTIONAL CONSEQUENCES*
,§,,,,¶,, and
Department of Physiology and Biophysics, and
¶ Department of Microbiology and Molecular Genetics, University of
California, Irvine, California 92697
*
This work was supported in part by National Institutes of
Health Grants GM54221 (to K. G. C.) and NS14609 (to M. D. C.), and by a gift from Merck Sharpe and Dohme (to K. G. C.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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 R. Kohler, S. Brakemeier, M. Kuhn, C. Behrens, R. Real, C. Degenhardt, H.-D. Orzechowski, A. R. Pries, M. Paul, and J. Hoyer Impaired Hyperpolarization in Regenerated Endothelium After Balloon Catheter Injury Circ. Res., July 20, 2001; 89(2): 174 - 179. [Abstract] [Full Text] [PDF]
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